Human respiration consists of mechanical ventilation and capillary gas exchange. Mechanical ventilation refers to the ventilatory cycle of breathing, that is, the inspiration and expiration (or inhalation and exhalation) of air, which will be referred to herein as the ventilatory “cycle.” Gas exchange refers to the exchange of oxygen and carbon dioxide between the lungs and the bloodstream.
Sleep apnea, a prevalent sleep disorder, manifests many ventilatory cycle disorders and other undesirable symptoms that range from snoring, breathing cessation, and headaches to depression, memory loss, and exacerbation of heart disease. “Hypopnea,” a related malady that begets some of the same symptoms as apnea, refers to a breathing rate or tidal volume that is less than approximately fifty percent of a patient's normal baseline breathing pattern. The term “apnea” is often applied loosely to refer to any combination of sleep apnea and hypopnea.
It can be difficult to properly detect apnea and hypopnea, quantify their occurrence, and respond to long-term trend changes in these maladies. Implantable devices are generally not equipped with the pattern recognition capability, computational power, and memory to properly diagnose and efficiently store long-term apnea and hypopnea data gathered in raw form from a host patient. Apnea manifests itself as a complex and variable pathology that conventionally requires great computational intensity to automatically monitor and treat.
Blood chemistry changes occur when apnea and hypopnea modify normal breathing during sleep. Breathing difficulty can cause blood oxygenation to fall to low levels and carbon dioxide and its derivatives to build up in the blood. When respiratory control centers in the brain sense these chemical changes, they often direct an arousal of the apneic patient. Thereafter, regular breathing and normal exchange of oxygen and accumulated carbon dioxide may resume—for a time—until the next episode. Severe apnea and hypopnea can result in hundreds of episodes of low blood oxygen levels per night. The typical apnea patient may have little awareness of the nightly struggle to breathe until its effects are felt the next day.
Sleep apnea can be classified as “obstructive” if caused by mechanical blockage of airflow, “central” if caused by a central nervous system disorder, and “mixed” if it is a combination of the obstructive and central types.
Sleep apnea can be life-threatening if it occurs with coronary artery disease (CAD) or congestive heart failure (CHF—sometimes referred to as just “heart failure”). CHF is a condition in which a weakened heart cannot provide enough pressure to prevent buildup of fluid in bodily tissues. CHF may affect either the right side, left side, or both sides of the heart. The weak pumping action causes fluid to back up into other areas of the body including the liver, gastrointestinal tract, and extremities (right-sided heart failure), or the lungs (left-sided heart failure). Heart failure patients have characteristic pulmonary edema or pitting edema of the lower legs.
Structural and functional causes of heart failure include high blood pressure (hypertension), valvular heart disease, congenital heart disease, cardiomyopathy, heart tumor, and other heart diseases. Precipitating and exacerbating factors include infections with high fever, anemia, irregular heartbeats (arrhythmias), hyperthyroidism, and kidney disease, and of course, sleep apnea. CHF and sleep apnea often occur together in a patient, as mentioned above, and they make each other worse. Treating one usually improves the other.
Not only does apnea place a load on the heart and cardiopulmonary system directly, but indirectly affects these organs by circumventing restful sleep. Sleep debt and daytime weariness resulting from the apnea worsen CAD, CHF, and hypertension. Consequently, sleep apneics who have a blood oxygen level lowered by sleep-disordered breathing are at increasing risk for hypertension, arrhythmias, heart attack, and stroke.
Approximately fifty percent of patients with heart failure suffer concurrent sleep apnea. About ten percent of these heart failure patients suffer from obstructive sleep apnea, while about forty percent suffer from central sleep apnea. A high comorbidity exists between sleep apnea and CHF, which results from a negative synergy between problematic gas exchange during apnea and problematic oxygen distribution characteristic of CHF.
It is generally believed that reducing heart failure symptoms reduces apnea, which in turn further reduces the heart failure symptoms. Therapy administered by an implantable device for diagnosing and treating sleep apnea is still relatively unexplored. Hence, there is a continuing need to improve the techniques for detecting and quantifying apnea while conserving the memory and computational resources of an implantable device.